Endotoxin-induced uveitis in the rat. The significance of intraocular interleukin-6.

The potential role of interleukin-6 (IL-6) was studied as an inflammatory mediator of endotoxin (or lipopolysaccharide [LPS])-induced uveitis (EIU) in the rat. In young Lewis rats, levels of intraocular IL-6, but not serum IL-6, correlated with the severity of uveitis and with aqueous humor protein levels in response to foot pad injections of LPS (P less than 0.001). Adult Lewis rats did not develop uveitis and had no intraocular IL-6, although IL-6 was released systemically. Resistance to EIU and absence of IL-6 levels in the aqueous humor, despite the ability to release serum IL-6, also were observed in brown Norway rats, irrespective of age and weight. Intravitreal injection of as little as 1 ng of human recombinant IL-6 induced uveitis in young Lewis rats. In adult Lewis rats, and in young animals made tolerant to LPS, intravitreal IL-6 still caused substantial leakage of plasma proteins into the anterior chamber but no influx of inflammatory cells. As early as 2 hr after intravitreal injection of IL-6, immunohistochemical analysis showed invasion of the iris, corneal stroma, and anterior chamber by polymorphonuclear leukocytes (PMN) and expression of major histocompatibility complex (MHC) class II antigen in the retina by large cells that were macrophage-marker ED2 negative. This was followed by massive PMN infiltration of the retinal layers and vitreous. The MHC class II antigen expression of ciliary and iris epithelium occurred at a later stage (greater than 8 hr).(ABSTRACT TRUNCATED AT 250 WORDS)     

AL-2512, a novel corticosteroid: preclinical assessment of anti-inflammatory and ocular hypertensive effects.

The anti-inflammatory efficacy and ocular hypertensive effect of AL-2512 were characterized in rodent and feline models of ocular inflammation. Neutrophil influx into ocular tissue following topical ocular administration of test drugs was evaluated in models of endotoxin-induced uveitis. In rats, the anti-inflammatory efficacy of AL-2512 was compared with that of 0.1% dexamethasone. Test drug or vehicle was administered topically before subplantar injection of endotoxin. Neutrophil influx was assessed at 24 hours. Feline eyes, injected intravitreally with endotoxin, were treated topically with 0.1% AL-2512, 1.0% prednisolone acetate or vehicle at various timepoints before and after endotoxin injection. At 12 hours, protein concentration and leukocyte count in aqueous humor were determined. In the feline intraocular pressure (IOP) model, after baseline IOP values were established, AL-2512, dexamethasone, or vehicle was administered topically to both eyes of cats. IOP was measured daily before and during treatment. Topical ocular administration of AL-2512 inhibited endotoxin-induced leukocyte influx in rodent and feline models of uveitis. In rats, AL-2512 significantly inhibited neutrophil influx by 89%, compared with 93% by dexamethasone. In feline eyes, AL-2512 significantly (p < 0.05) inhibited leukocyte infiltration of aqueous humor by 59%, compared to 37% inhibition by prednisolone acetate. Intraocular pressure in cats treated for 32 days with AL-2512 or dexamethasone increased 6% and 18%, respectively. The ocular anti-inflammatory effect of AL-2512 was equivalent to dexamethasone and superior to prednisolone acetate in rat and feline models of ocular inflammation, respectively. This steroid provides anti-inflammatory efficacy equivalent to dexamethasone with a reduced risk of inducing ocular hypertension.     

Intraocular antibody synthesis during experimental uveitis

Determination of intraocular antibody synthesis against certain microorganisms is a diagnostic aid in identifying the causative agent in clinical uveitis. Little is known, however, concerning the kinetics and specificity of antibodies produced during intraocular inflammation. To investigate this subject we induced uveitis in rabbits by injecting small amounts of human serum albumin (HSA) into the vitreous. Aqueous humor and serum were taken before and after the induction of uveitis and levels of total IgG, rabbit albumin and anti-HSA-IgG were determined. The anti-HSA-IgG was quantitated using immunoaffinity purified anti-HSA-IgG as a standard. Six weeks after intravitreal HSA injection, high levels of total IgG (4.7 mg/ml) and albumin (15.4 mg/ml) were observed in the aqueous as compared to control eyes (IgG: 0.12 mg/ml; albumin: 0.48 mg/ml). Using albumin to correct for blood aqueous barrier breakdown we calculated that only 0.6% of the locally synthesized IgG was directed against intravitreally injected HSA. Two months after the intravitreal injection of HSA the main signs of the uveitis had subsided. A recurrent uveitis was subsequently induced by an intravenous HSA injection. This resulted in a marked increase of total IgG (14.3 mg/ml) and albumin (24.6 mg/ml) in the aqueous humor of the uveitis eyes. It was remarkable that the mean anti-HSA-IgG level (0.62 mg/ml) in the uveitis eyes was higher than that seen in serum (0.41 mg/ml). After this secondary uveitis, 9% of the locally synthesized antibodies were directed against HSA.(ABSTRACT TRUNCATED AT 250 WORDS)     

The influence of topical corticosteroid therapy upon polymorphonuclear leukocyte distribution, vascular integrity and ascorbate levels in endotoxin-induced inflammation of the rabbit eye

An acute inflammatory response was initiated in the rabbit eye by an intravitreal injection of bacterial endotoxin. We examined the effect of topical corticosteroid therapy upon polymorphonuclear leukocyte (PMN) infiltration into the eye, protein leakage into aqueous humor and ascorbate level in aqueous humor. Corticosteroid therapy initiated prior to injection of endotoxin suppresses the clinical signs of inflammation, partially prevents the fall in aqueous-humor ascorbate level, has little effect upon protein leakage, but markedly reduces PMN infiltration. Corticosteroid therapy initiated after the injection of endotoxin also suppresses the clinical signs of inflammation, reduces the fall in ascorbate levels and does not influence protein leakage. However, in this case there is a marked persistence of PMN infiltration into ocular tissues. Thus the number of PMNs present in the ocular tissues is little different from that in non-steroid treated control eyes, although the clinical signs of inflammation are reduced. We suggest that in the clinical situation, the initial anti-inflammatory activity of the corticosteroids is related to an inhibitory effect upon the activity of PMNs already within the tissues, which then prevents the ensuing cascade of characteristic inflammatory events.     

Ferroxidase activity increases in the aqueous humor during the ocular inflammatory response

Ferroxidase activity was increased in the aqueous humor from inflamed eyes compared to their uninflamed contralateral controls 24 h after intravitreal injection of 10 ng of endotoxin. Changes in ferroxidase activity and copper concentration paralleled each other indicating that the plasma copper transport protein ceruloplasmin (plasma ferroxidase) entered the inflamed aqueous humor from plasma through disrupted blood ocular barriers. The presence of ferroxidase activity would facilitate the removal of potentially damaging, free radical generating Fe+2. Therefore, plasma proteins may perform important protective functions in the inflamed intraocular fluids.     

Integrity of the blood-aqueous barrier in hyperuricemia

Neither the origin nor the role of high levels of uric acid, found in the aqueous humor of some human glaucomatous eyes, is known. A model of hyperuricemia in the rat was evaluated for its contribution to urate levels in the aqueous humor. Epinephrine-induced hyperuricemia in male rats was shown to increase mean serum urate levels from 1.2 mg/dL to 6.7 mg/dL. Female rats were shown to have a lower uric acid baseline and a lower absolute hyperuricemic level than males. The mean aqueous-humor urate levels were increased from 0.06 mg/dL to 0.33 mg/dL for male rats. In our studies, the blood-aqueous barrier effectively prevented equilibration between the systemic and ocular compartments. The increased aqueous-humor uric acid levels in glaucoma may arise from intraocular mechanisms.     

Ocular responses to superoxide generated by intraocular injection of xanthine oxidase

Xanthine oxidase (XaO) was injected into the anterior chamber of rabbit eyes by a closed circuit perfusion system. Doses of 1.5 milliunits (mU) or greater produced a maximal leucocyte accumulation after 4 hr, with an initial elevation of ocular pressure in the first 15 min. Similar experiments on rats with intravitreal injections of 0.1-1.5 mU of XaO resulted in a significant accumulation of leucocytes after 5 hr which, at the highest dose of XaO, was partly due to traces of bacterial endotoxin in the XaO. However, in endotoxin-desensitized rats the response to 1.5 milliunits XaO was seven-fold greater than the response to endotoxin alone. Simultaneous administration of xanthine (Xa) substrate with XaO was not required to elicit cell infiltration into the anterior chamber. Dialyzed enzyme was also effective but boiling abolished the response. Addition of XaO to rabbit aqueous humor in vitro decreased the ascorbate content, consistent with the generation of superoxide from an endogenous substrate. The results suggest that enzymatically active XaO, which can cause intraocular generation of superoxide from an XaO substrate present in aqueous humor, initiates the chemotactic response. A chemotactic agent may be generated from superoxide reacting with endogenous precursors in aqueous humor or by selective activation of the lipoxygenase pathway of arachidonic acid metabolism in adjacent tissues.     

Time course of rabbit ocular inflammatory response and mediator release after intravitreal endotoxin

An inflammatory response was elicited in the rabbit eye by intravitreal injection of endotoxin. The appearance in aqueous humor of selected metabolites of arachidonic acid metabolism at various times was correlated with the influx of protein and myeloperoxidase activity in the iris-ciliary body. After intravitreal injection of endotoxin, aqueous humor protein levels increased substantially within 2 hr. This aqueous humor protein increase occurred before a significant appearance of prostaglandin E2 (PGE2) in the aqueous humor. Myeloperoxidase activity in the iris-ciliary body, a measure of polymorphonuclear leukocyte (PMN) infiltration, showed little elevation until 6 hr after endotoxin injection and then increased rapidly through 24 hr. The appearance of the leukotriene B4 (LTB4) followed a similar time course: levels in the aqueous humor were partially elevated until 6 hr after endotoxin injection, when levels begin to rise rapidly. These findings are interpreted to demonstrate the dependence of PMN infiltration on the release and accumulation of LTB4; the initial breakdown of the blood-aqueous barrier and influx of protein appears to be independent of significant release of PGE2.     

The pathophysiology of the ocular microenvironment. II. Copper-induced ocular inflammation and hypotony

The ocular effects of intravitreally injected copper sulfate solutions were studied in New Zealand white rabbits. These injections resulted in uveitis characterized by prolonged ocular hypotony, increased protein concentrations and decreased ascorbic acid concentrations in both the vitreous and aqueous humors, and an apparent decrease in the transport function of the anterior uvea. The extent and the duration of these effects were dose-dependent. The lower doses used, 3 or 6 micrograms of Cu as CuSO4 per eye, produced reversible inflammation. The highest dose, 30 micrograms of Cu per eye, also produced some signs of ocular chalcosis: hemorrhage, vitreous liquefaction, prolonged hypotony and local iridial ischemia. Six hours after the intravitreal injection of 6 micrograms of Cu as CuSO4 per eye, the Cu concentration in the vitreous humor increased to approximately 100 times that in the vitreous of control eyes, and began to decline only 3 days later, with a half-time of approximately 8 days. The Cu concentration in the anterior chamber of these eyes never exceeded 1 ppm and returned close to control values within 3 days. Based on these findings, factors that affect ocular trace-metal distribution and kinetics are discussed, as are reasons for the apparent difficulty in diagnosing the presence of Cu-containing intraocular foreign bodies on the basis of the Cu concentration of the aqueous humor.     

内源性眼内炎的临床特征及治疗

目的：探讨内源性眼内炎的临床特征及治疗。方法：对2005/2011年所收治的内源性眼内炎患者8例进行常规眼科检查,取前房水及玻璃体标本涂片和培养,血培养。给予局部及全身抗菌药物治疗,行玻璃体注药或（和）玻璃体切割术。观察病变特点及治疗效果。结果：患者8例9眼中男6例7眼,女2例2眼,年龄45～78岁。患者可有前葡萄膜炎症表现,玻璃体炎性改变,5例患者病原菌培养阳性,3眼行玻璃体腔注射,6眼行玻璃体切割手术。经治疗,患者病情控制,6眼视力提高。结论：内源性眼内炎根据病史、危险因素、临床表现以及实验室检查等综合进行诊断。局部＋全身治疗可有效控制感染。     

Effects of intravitreal injection of tacrolimus (FK506) in experimental uveitis

PURPOSE: To examine the immunosuppressive and neuroprotective effects of intravitreal injection of tacrolimus in experimental uveitis. METHODS: Tacrolimus (40 microg) was injected intravitreally in rabbits to examine safety. Experimental uveitis was induced in rabbits by systemic immunization with bovine serum albumin (BSA) followed by intravitreal challenge with BSA. On day 1 after BSA challenge, tacrolimus (20 or 40 microg) or betamethasone (400 microg) was injected intravitreally in one eye and balanced salt solution in the contralateral eye. The eyes were evaluated by slit-lamp biomicroscopy, electroretinography, and histopathology. RESULTS: No local or systemic adverse reaction was observed in normal rabbits. In experimental uveitis, intravitreal injection of tacrolimus significantly reduced intraocular inflammation in histopathological analysis (p < 0.03). Amplitudes on the electroretinogram were restored (p < 0.01), and retinal thickness was preserved in tacrolimus-treated eyes (p < 0.03). CONCLUSIONS: In experimental uveitis, intravitreal injection of tacrolimus effectively suppresses ocular inflammation and preserves retinal architecture.     

The ocular hypotensive effects of demeclocycline, tetracycline and other tetracycline derivatives

Demeclocycline, tetracycline and other tetracycline derivatives lowered intraocular pressure (IOP) in rabbits following intravitreal injection, but the onset of this effect was not evident until 1 or more days after drug administration. Of the drugs tested, demeclocycline was the most active ocular hypotensive agent. Demeclocycline caused a dose-dependent decrease in IOP. The maximum IOP decrease of approximately 12 mm Hg occurred 5 days after intravitreal administration of 0.5 mg, with the effect persisting for over a week. Demeclocycline did not alter tonographically measured aqueous humor outflow facility or episcleral venous pressure. Based on calculated aqueous humor flow rates following 0.2 mg demeclocycline, a 62% decrease in aqueous humor formation occurred 7 days after intravitreal injection. The flow-to-diffusion ratio for ascorbate was reduced 54% 6 days after the intravitreal administration of demeclocycline, a change also consistent with suppression of aqueous humor formation. Anterior chamber aqueous humor protein concentration was increased 6 days after demeclocycline administration. No histologic changes were present in the treated eyes by light microscopy. Intravitreal demeclocycline similarly lowered IOP in cats, with the duration of effect lasting up to 20 days.     

白细胞介素-10对内毒素诱导的实验性葡萄膜炎的治疗作用

目的 观察重组白细胞介素10(IL-10)对大肠杆菌内毒素(LPS)诱导的实验性葡萄膜炎(EIU)的治疗作用.方法 雄性Wistar大鼠56只随机分为3组,其中IL-10治疗组和阳性对照组各24只,正常对照组8只.治疗组和阳性对照组大鼠用LPS诱导EIU模型,治疗组24只大鼠在注射LPS前4.0、0.5 h分别按1μg/kg的剂量经尾静脉注射重组IL-10各1次,正常对照组大鼠同一部位注射等量生理盐水.阳性对照组和正常对照组大鼠用于对比观察.注射LPS后观察大鼠的发病开始时间和眼部表现,分别在注射LPS后4、24 h和3 d等3个时间点分批处理8只大鼠后取血和房水,检测血清和房水中肿瘤坏死因子(TNF)α、IL-6和IL-10水平,并进行病理检查和分级.结果 阳性对照组24只大鼠全部出现葡萄膜炎反应,平均发病开始时间为(3.81±1.05)h,平均炎症评分为3.67±1.97,平均组织病理学分级为3.08±1.77.治疗组24只大鼠也全部出现轻度葡萄膜炎反应,平均发病开始时间为(5.63±1.02)h,平均炎症评分为2.00±1.25,平均组织病理学分级为1.67±1.17.治疗组大鼠的发病开始时间明显迟于阳性对照组大鼠(t=4.95,P=0.00),炎症评分(t=3.50,P=0.00)和组织病理学分级(t=3.28,P=0.00)也显著低于阳性对照组.正常对照组8只大鼠始终无阳性体征及病理改变.阳性对照组大鼠血清、房水TNF-α和IL-6水平明显高于治疗组和正常对照组(F=15.34,57.65,67.59,8.42;P=0.00),治疗组大鼠血清和房水IL-10水平明显高于阳性对照组和正常对照组(F=17.84,7.76;P=0.00).房水TNF-α、房水和血清IL-6与眼部炎症程度呈正相关(眼部表现评分r=0.58,0.31,0.81;组织病理学分级r=0.56,0.31,0.74;P=0.00);血清IL-10与炎症程度呈负相关(眼部评分和组织病理学分级分别为r=-0.54,-0.55;P=0.00),与发病开始时间呈正相关(r=0.73,P=0.00);血清及房水TNF-α和IL-6水平与发病开始时间呈负相关(r=-0.47,-0.59,-0.77,-0.36;P＜0.05).结论 IL-10能显著抑制LPS诱导的EIU模型中前炎症因子TNF-α和IL-6产生,减轻EIU眼部表现和病理损害,具有治疗EIU的作用.     

Comparison of uveitis induced by interleukin-8 (IL-8) and endotoxin in rabbits

IL-8 is a potent chemoattractant which has been postulated to play a role in the cytokine cascade associated with uveitis. The authors studied the effect of intravitreal IL-8 on the induction of uveitis in the rabbit. IL-8 at varying concentrations (1 ng, 10 ng or 100 ng) or endotoxin (100 ng) was injected intravitreally within the rabbit eye. At 6, 24 and 48 hours following injection the induction of uveitis was evaluated by clinical scoring, anterior chamber (AC) leukocyte count, AC protein concentration and histopathology in 15 rabbits. Only the 100 ng concentration of IL-8 induced uveitis at 6 and 24 hours by clinical scoring and AC leukocyte count; the AC protein concentration remained normal. In contrast, endotoxin caused a severe uveitis with a significant increase in all the parameters evaluated. The authors conclude that intravitreal IL-8, in the concentrations studied, induces a limited uveitis which is detectable at six hours and resolves within 48 hours. It is characterized by leukocyte infiltration without an increased AC protein concentration. Thus, IL-8 may play a role in the cytokine cascade involved in the induction of uveitis.     

Comparison of uveitis induced by interleukin-8 (IL-8) and endotoxin in rabbits

IL-8 is a potent chemoattractant which has been postulated to play a role in the cytokine cascade associated with uveitis. The authors studied the effect of intravitreal IL-8 on the induction of uveitis in the rabbit. IL-8 at varying concentrations (1 ng, 10 ng or 100 ng) or endotoxin (100 ng) was injected intravitreally within the rabbit eye. At 6, 24 and 48 hours following injection the induction of uveitis was evaluated by clinical scoring, anterior chamber (AC) leukocyte count, AC protein concentration and histopathology in 15 rabbits. Only the 100 ng concentration of IL-8 induced uveitis at 6 and 24 hours by clinical scoring and AC leukocyte count; the AC protein concentration remained normal. In contrast, endotoxin caused a severe uveitis with a significant increase in all the parameters evaluated. The authors conclude that intravitreal IL-8, in the concentrations studied, induces a limited uveitis which is detectable at six hours and resolves within 48 hours. It is characterized by leukocyte infiltration without an increased AC protein concentration. Thus, IL-8 may play a role in the cytokine cascade involved in the induction of uveitis     

Complications of intravitreal injections--own experience

PURPOSE: Authors present complications associated with intravitreal injection perfomed in Ophthalmic Clinic CMKP MATERIAL AND METHODS: retrospective study, between January 2006 and July 2009 we performed intravitreal injections with triamcinolone acetonide (Kenalog, 4 mg), ranibizumab (Lucentis, 0.5 mg), bevacizumab (Avastin, 1.25 mg) and pegaptanib (Macugen, 0.3 mg). We treated eyes with age-related macular degeneration, diabetic macular edema, after retinal venous occlusion, with uveitis, Irvine-Gass syndrome, idiopathic juxtafoveolar teleangiectasia and central serous retinopathy. RESULTS: 943 eyes received intravitreal injections. The most common ocular complication was subconjunctival hemorrhage which was seen in 36% cases. Temporary elevated intraocular pressure above 21 mmHg was noticed in 18 eyes (5%) after anti-VEGF agents injections and in 30 eyes (23.4%) after Kenalog injection. Anterior uveitis developed in sixteen cases (1.7%) from the Avastin (5 eyes) and Lucentis (3 eyes) group. Anterior-posterior inflammation occurred in 8 eyes (0.8%), including four eyes (0.4%) with sterile endophthalmitis (3 following bevacizumab and 1 following ranibizumab injection), one eye (0.1%) with pseudoendophthalmitis (after triamcinolone). There were three cases of suspected endophthalmitis (2 following bevacizumab and 1 following triamcinolone injection). The infectious endophthalmitis after triamcinolone injection was culture-proven and revealed Staphylococcus epidermidis. Cataract formation or progression was noted in 34 eyes totally. In Kenalog group progression of cataract was seen in 23.4% of eyes (30 cases) during 2-years of follow-up and in anti-VEGF agents group--in two cases (0.6%) and 2 cases of iatrogenic cataract. Three diabetic patients suffered systemic adverse events: one patient developed renal insufficiency, one patient developed cerebrovascular accidents and one suffered a myocardial infarction resulting in death. Conclusions: Intravitreal injections are associated with a low incidence of serious adverse events. The most common ocular complication was subconjunctival hemorrhage. There was one case of serious complication--the culture-proven infectious endophthalmitis after Kenalog injection. Cataract formation and increase of intraocular pressure were more often observed following intravitreal triamcinolone injection.     

Endotoxin-induced uveitis in rats: morphological and biochemical study

Inflammation induced by systemic injection of endotoxin can be a good model for endogenous uveitis since ocular inflammation is induced without manipulating the eye. We carried out morphological and biochemical studies in Lewis rats to evaluate the breakdown of the blood-ocular barrier following injection of endotoxin (1 mg/rat) in footpads. Vasodilation was observed as early as 3 hours and became maximum at 18-24 hours after the injection. Unlike in the eye, no inflammatory changes were observed in other organs. Protein and cell contents in the aqueous humor increased significantly as early as 3 hours after the injection and reached a peak level at 24 hours. The protein content returned to the normal level in the following several days, while cells in the aqueous humor remained at a high level even 1 week after the injection. The time-course of the pupillary size was very similar to that of the protein concentration. Furthermore, we examined leukotrienes (LTs) levels in aqueous humor by high-pressure liquid chromatography. LTD4 was detected in the aqueous humor at 6 hours and reached its peak level at 24 hours. The present data indicates that the systemic injection of endotoxin causes the disruption of the blood-ocular barrier soon after the injection and inflammation becomes maximum in 18-24 hours. This model can be used for studying endogenous uveitis and the disruption of the blood-ocular barrier without direct trauma to the eye.     

The insensitivity of the chicken eye to the inflammatory effects of x-rays in contrast to its sensitivity to other inflammatory agents.

The effects of x-rays and three chemical agents, known to cause intraocular inflammation in mammalian eyes, were studied on the chicken eye because this species was reported to be insensitive to the cataractogenic effects of x-rays. Intravitreal injection of Shigella endotoxin and topical and/or intravitreal administration of PGE2, PGF2alpha, or arachidonic acid caused a breakdown of the blood-aqueous barrier, as indicated by flare and increased protein concentration in the aqueous humor. Following endotoxin injection, there was also a large accumulation of cells in the anterior chamber. The ocular inflammatory effects of endotoxin and arachidonic acid were inhibited by indomethacin. Thus the chicken eye reacts to these inflammatory agents in a manner similar to that previously described for the rabbit. In contrast, the inflammatory response which was reported to occur in the rabbit eye 3 to 4 hr after exposure to 500 or 1000 rads of x-rays was not observed in the chicken eye even after expsoure to 10,000 rads. Minimal flare and a small cellular infiltration were observed in some eyes only after extensive swelling of the surrounding tissues had developed. It is concluded that the insensitivity of the chicken eye to x-rays is due to some unique difference in the chain of events which mediates, or prevents, the effects of ionizing radiation rather than to a general insensivity to inflammatory agents.     

Intravitreal triamcinolone acetonide for treatment of intraocular proliferative, exudative, and neovascular diseases

Within the last three years, triamcinolone acetonide has increasingly been applied intravitreally as treatment option for various intraocular neovascular edematous and proliferative disorders. The best response in terms of gain in visual acuity after the intravitreal injection of triamcinolone acetonide was found in eyes with intraretinal edematous diseases such as diffuse diabetic macular edema, branch retinal vein occlusion, central retinal vein occlusion, and pseudophakic cystoid macular edema. Visual acuity increased and degree of intraocular inflammation decreased in eyes with various types of non-infectious uveitis including acute or chronic sympathetic ophthalmia and Adamantiadis-Behcet's disease. Intravitreal triamcinolone may be useful as angiostatic therapy in eyes with iris neovascularization and proliferative ischemic retinopathies. Possibly, intravitreal triamcinolone may be helpful as adjunct therapy for exudative age-related macular degeneration, possibly in combination with photodynamic therapy. In eyes with chronic, therapy resistant, ocular hypotony, intravitreal triamcinolone can induce an increase in intraocular pressure and may stabilize the eye. The complications of intravitreal triamcinolone therapy include secondary ocular hypertension in about 40% of the eyes injected, cataractogenesis, postoperative infectious and non-infectious endophthalmitis, and pseudo-endophthalmitis. Intravitreal triamcinolone injection can be combined with other intraocular surgeries including cataract surgery. Cataract surgery performed some months after the injection does not show a markedly elevated rate of complications. If vision increases and eventually decreases again after an intravitreal triamcinolone acetonide injection, the injection can be repeated. The duration of the effect of a single intravitreal injection of triamcinolone depended on the dosage given. Given in a dosage of about 20mg to non-vitrectomized eyes, the duration of the effect and of the side-effects was 6-9 months. Intravitreal triamcinolone acetonide may offer a possibility for adjunctive treatment of intraocular edematous and neovascular disorders. One has to take into account the side-effects and the lack of long-term follow-up observations.